A new study authored by psychiatrist Dr. Theodore Henderson, and published this week in Frontiers in Psychiatry, shows a breakthrough in treating depression, particularly for patients with traumatic brain injury (TBI).

The observational study, “Multi-Watt Near-Infrared Phototherapy for the Treatment of Comorbid Depression: An Open Label Single-Arm Study,” describes 39 patients who had both traumatic brain injury (TBI) and depression. After being treated with a revolutionary new treatment developed by Drs. Henderson and Morries, a staggering 82 percent of the patients from the study report being in remission – no longer having the symptoms of depression.

Patients receiving the NILT treatment sit or lay comfortably during a series of 20-35 minute sessions in which the neuro-laser is applied by trained medical professionals. There is no skin irritation, pain, or unpleasant feelings. There are no other side effects, which have always been the downside of antidepressant medication including weight gain, drowsiness, even erectile dysfunction.

Dr. Henderson warns consumers about other “laser” treatments, as typically they feature a “low-level” source which does not have any therapeutic effect. The device used in this study, which is the only one available for clinical use, features a high-powered, and multi-Watt near-infrared light (NILT).

Learn more at Ketamine Infusion Centersor schedule a consultation by calling 855-978-0808 or send email to nlbrainhealth@gmail.com

Attend the TBI Gala April 30th 2017

March is TBI awareness month. With politics dominate the newscasts these days, we might forget that every day at least 20 veterans commit suicide. Many believe posttraumatic stress disorder (PTSD), and traumatic brain injury (TBI) have a significant contribution to the sense of despair and futility that lead these veterans to take their own lives. For the proud warrior, depression, anxiety, or the hopelessness of a diagnosis of TBI may contribute to their choice to end their life. In addition, veterans with PTSD or depression are often reluctant to seek help because they feel PTSD and depression are not real brain disorders, but a failure of character. Fear of medications and a lack of confidence in the therapies offered by the Veterans Administration are also factors that keep veterans isolated and untreated.1-3

Recently, Dr. Henderson published a scientific paper reporting on the real-world experience for his patients receiving ketamine infusions for the treatment of persistent depression. All of these patients had failed five or more antidepressants before receiving intravenous infusions of ketamine delivered over 40 minutes or more. Dr. Henderson has treated over 320 patients so far, but only 100 had consented to using their data for research study. Among those 100 (roughly half were female and mean age was 41 years), 80% experienced improved mood. Notably, Dr. Henderson’s approach results in prolonged improvement in mood. Read the entire study at Henderson_ketamine_study. Several news stories have been written about this study and Dr. Henderson has been interviewed world-wide about his findings. Here is a recent news article ketamine in the news.

Molecular neuroimaging using single-photon emission computed tomography (SPECT) has allowed for direct visualization of functional systems in the living human brain. DaTSCAN is a radiopharmaceutical approved 2 years ago by the FDA with indications for “striatal dopamine transporter visualization using SPECT brain imaging to assist in the evaluation of adult patients with suspected Parkinsonian syndromes.” In these patients, DaTSCAN may be used to help differentiate essential tremor from tremor resulting from one of the parkinsonian syndromes (IDP, MSA, PSP). DaTSCAN is an adjunct to other diagnostic evaluations.

Dopamine Transporter (DAT) Imaging

DAT imaging offers certain advantages. First, DAT is largely limited to presynaptic membranes which, in the striatum, are predominantly the axonal terminals of substantia nigra neurons. Therefore, DAT allows direct visualization of the integrity of the neurons that appear most vulnerable to degeneration in IPD. Second, a minimum of metabolic processing, and therefore shorter incubation time during imaging, is possible.

Two derivatives are approved in Europe: I 123 beta CIT, marketed as Dopascan, and I123 Ioflupane, marketed as DaTSCAN. The DaTSCAN has been in use in Europe for 12 years, giving our European colleagues extensive experience with making full use of this marker.

The Value of Quantitative Analysis

One observation, based on the extensive experience in Europe, has been the value of quantitative or semiquantitative analysis. Visual interpretation of the DaTSCAN does not make full use of its capabilities. For example, when specific binding ratios relative to the occipital cortex are quantified (such as provided with the Hermes BRASS system), a Z-score derived from a normal database can be calculated. This has utility in differentiating accurately between Parkinson disease, which typically has an asymmetric dopaminergic denervation in the putamen and caudate, and non-parkinsonian causes of tremor, which show nonsignificant Z-scores. Such causes of tremor include medications and essential tremor.

Quantitative DaTSCAN analysis also is critical in the case of the positive DaTSCAN to assist in differentiation of IPD and other parkinsonian syndromes (MSA, DLB, PSP) that tend to have a symmetrical denervation. However, DaTSCAN cannot reliably distinguish these parkinsonian syndromes alone.

Despite recent work by President Carter’s wife Rosalyn, and daily reports of the prevalence of mental illness, unfortunately still many people associate a negative stigma with the often mysterious conditions resulting from the brain. Yet, we are all susceptible to mental illness.

During this first week of October, which is “Mental Illness Awareness Week,” I would hope people realize this year — more than any other — we have new hope for the treatment of depression, and other mental illnesses. But so many do not seek help due to stigma and misunderstanding of their conditions. Many patients have told me, “I did not seek help because I thought it was just psychological….that it was just because of my situation.”

But, we now know that genetics and other biological processes contribute to one’s vulnerability for depression and other illnesses. For example, researchers have found that a certain gene that regulates, the catechol-O-methyltransferase (COMT) enzyme, makes one more sensitive to trauma and more likely to develop post-traumatic stress disorder (PTSD). Other genetic variations also may contribute to being at risk for PTSD.

All in all, these data clearly show the mental illness is not a matter of choice. And, virtually anyone can be vulnerable. Rather, it results from a complex interplay between genetics, other biological risk factors, and experiences.

What are these other biological risk factors? It might surprise you to learn that often they are viruses. Recently, I published some research showing the relationship between viruses of the Herpes family (which include cytomegalovirus, Epstein-Barr virus, and Herpes 6 among others) and Chronic Fatigue Syndrome. Moreover, all of the patients in this retrospective case series had been referred to my practice with a diagnosis of treatment-resistant depression or mood disorder. This paper was recently summarized on a national CFS website.

So during this week, and every week of the year, remember that mental illness is not a matter of choice. A person cannot just pull themselves up by their bootstraps. Moreover, traditional psychiatric medications may not be the answer. Successfully treating depression may require an understanding of the genetics, determining if infectious agents are present, and treating these agents effectively.

Dr. Theodore Henderson of Neuro-Luminance will be presenting at the United States Autism and Asperger Association (USAAA) meeting this month. The USAAA meeting held in Kansas City, Missouri from September 4-7, 2014 is designed for persons with autism, their families and their clinicians. Dr. Henderson will be speaking on the psychopharmacology of comorbid conditions associated with autism. He will be integrating neuroimaging, sophisticated pharmacology, and a deep understanding of how the brain functions. In addition, he will be featured on professional panels on many aspects of autism. The entire USAAA conference, including Dr. Henderson’s talks will be recorded and available on the USAAA website.

On March 19, 2014, an international team led by Dr. Theodore Henderson published a comprehensive review of the utility of SPECT neuroimaging in the evaluation and treatment of traumatic brain injury (TBI). This review (Raji CA, Tarzwell R, Pavel D, Schneider H, Uszler M, et al. (2014) Clinical Utility of SPECT Neuroimaging in the Diagnosis and Treatment of Traumatic Brain Injury: A Systematic Review. PLoS ONE 9(3): e91088. doi:10.1371/journal.pone.0091088) published in PLos ONE, summarized data derived from research studies conducted over 30 years and involving 2,634 patients. Nineteen longitudinal studies involving 903 patients demonstrated the predictive value of SPECT neuroimaging for the clinical outcome of patients with TBI. The ability of a SPECT at the time of injury to predict persisting symptoms of TBI was 59%, but if the SPECT scan remained abnormal at three months the predictive value rose to 95%. SPECT scans have a high sensitivity for TBI (91%). If a SPECT scan at the time of injury is negative, then this predicts full recovery with an 89% accuracy. The article reviewed 52 cross-sectional research studies involving over 2100 patients and found that the frontal lobe was the most common area of injury occurring in 94% of patients with TBI. The temporal lobe was the second most common area injured (77%).

In studies comparing SPECT to more conventional neuroimaging techniques such as computed tomography (CT scan) or magnetic resonance imaging (MRI), SPECT proved far superior in detecting TBI in both the acute and chronic condition. Particularly in the case of mild TBI, also known as concussion, anatomical findings that can be picked up by CT or MRI are rarely present. Nevertheless persons with mild TBI are much greater risk of developing psychiatric symptoms, such as depression anxiety attention problems and impulse control problems. Indeed, many cases of treatment resistant depression proved to be undiagnosed TBI. The desperate need of patients suffering from TBI, concussion, or postconcussive syndrome is clearly illustrated by the shockingly high rate of suicide among soldiers returning from Afghanistan and Iraq. These brave soldiers who often serve their country on multiple tours of duty and often experienced one or more TBI’s did not die on the battlefield, but instead die in their own homes and in their own country by their own hand or as a result of substance abuse, homelessness, depression, and cognitive impairment. This national tragedy deserves to be addressed and the injury to the brains of these fine men and women should be one of America’s top priorities. If you or someone you know struggles with the aftermath of TBI, reach out to Neuro-Luminance for help in identifying and treating the brain injury.

Depression has been a vexing problem in Psychiatry. Our simplistic explanation of “too little serotonin” has hardly proven effective for most depression sufferers. In fact, some experts, such as Nassir Ghaemi, MD, noted expert on psychopharmacology recently wrote:

“Psychiatry… use(s) hundreds of made-up labels for professional purposes, without really getting at the reality of what is wrong with the patient…. (We have little understanding of) what the causes of those disease…We have a huge amount of neurobiology research now to conclude that the 20th century neurotransmitter theories of psychopharmacology basically are false.” (Nassir Ghaemi, MD, Psychiatry, Medscape Connect)

It seems that second messenger pathways actually are more important in treating depression. What an antidepressant does by raising serotonin or norepinephrine is hopefully activate one of these second messenger pathways. But the success of that medication depends upon genetics, enzymes, neurotrophic factors and many other variables. One of the key second messenger pathways is mediated by the chemical glutamate, acting on a particular receptor called the NMDA receptor. The NMDA receptor is involved in learning, memory, and plasticity of the brain. This glutamine receptor alters ion channels in brain cells and sets off a chain of secondary events, increasing brain growth factors and regenerative pathways. Ketamine, an anesthetic that has been in clinical use for many years, works very powerfully on the NMDA receptor. The result is a tremendous lifting of the depression in a great majority of cases. The relief of symptoms can begin almost immediately or over the next few hours.

Ketamine is a unique medication in the treatment for depression. It is not an SSRI, SNRI or a MAOI. Ketamine can be safely combined with most medications, so patients do not have to stop their current medications to begin ketamine.

We stand at an amazing historical moment in Psychiatry. As the new DSM-V (the diagnostic manual for Psychiatry) comes out, thought leaders in Psychiatry, Neuroscience, and brain research are questioning the very validity of psychiatric diagnoses. For example, Dr. Tom Insel, Director of the National Institutes of Mental Health, has announced that he believes the DSM system is broken and that federal agency will no longer be funding research based only on DSM diagnostic criteria. At the same time, I submitted a clinical paper on how Chronic Fatigue Syndrome (a virally-mediated disease) can be mistakenly diagnosed as Depression. I have now treated dozens of adults and adolescents who came to me with the diagnosis of “treatment-resistant depression” and instead they had Chronic Fatigue Syndrome. With proper treatment, this viral illness can be successfully controlled.

Now, more than ever, it is important to look at psychiatric illnesses with new eyes. We need to utilize neuroimaging, genetic testing, immunological testing, laboratory studies and a thorough understanding of the neurobiological basis of disease. Only then, can we determine how to correctly treat a patient. The answer does not come from a book of pigeon-holes into which we try to make patients fit. The answer comes from a comprehensive diagnostic work-up of the patient and their brain. To learn more about this new way to think about you, your brain, and your mental health, please visit Neuro-Luminance.

Dr Henderson is in private practice in Denver, Colorado. He is a board member of the Brain Imaging Council of the Society of Nuclear Medicine and President of The Synaptic Space, a neuroimaging consulting firm, in Centennial, Colorado.

The recent commentary by Dr Ronald Pies concerning the changes in the diagnostic criteria for Alzheimer’s disease (AD) and Mild Cognitive Impairment (MCI), questioned the value of informing a patient early in the course of a dementing illness……

While there are currently no treatments for AD, it is important to examine what we are treating. By the time AD is diagnosed by clinical symptoms, 8 to possibly 15 years of pathological damage has already occurred. Just as in Parkinson’s disease wherein over 80% of the substantia nigra neurons must be lost before symptoms manifest, the AD-related damage to the entorhinal cortex, hippocampus, and parietal cortex are much advanced by the time a drop in the Mini-Mental-Status Examination score occurs. Treatment at this point cannot undo the pathological damage. Therapeutic interventions, to be effective, must be introduced as early as possible in the pathological process.

Perfusion SPECT neuroimaging can identify MCI with an accuracy of as high as 99%.2-5 Amyloid markers can differentiate AD from controls with 85% to 95% sensitivity and 91% to 100% specificity in advanced cases.6-9 But these markers can also identify MCI with 80 % sensitivity and 90% specificity10; however, it must be noted that 10% of controls aged 50 years have a positive amyloid scan. This false positive rate increases by 10% each decade.6 Nonetheless, neuroimaging provides an endophenotype which can be quantified and detected long before the patient begins to show the cognitive dysfunction of AD or MCI. The implications are tremendous, not just in terms of early intervention, but also in terms of speeding clinical trials. Currently, we must wait years to see if a therapeutic intervention is making a difference……